Use of immune modulators to improve nerve regeneration

Abstract

The present disclosure describes the use of immune modulators to promote nerve growth and regeneration, particularly in the context of nerve deficit stemming from trauma and disease. In particular, the disclosure provides for the use of of CXCR4 antagonsists, STAT3 activators, and an agent that increase nitric oxide, alone or in combination, to treat nerve deficit conditions.

1 . A method of increasing nerve growth, regrowth or regeneration in a subject comprising administering to said subject a CXCR4 antagonist, a STAT3 activator, and/or an agent that increases nitric oxide content. 
     
     
         2 . (canceled) 
     
     
         3 . (canceled) 
     
     
         4 . The method of claims  1  or  2 , wherein administering comprises administering a CXCR4 antagonist with a STAT3 activator. 
     
     
         5 . The method of claims  1  or  2 , wherein administering comprises administering a CXC4 antagonist with an agent that increases nitric oxide content. 
     
     
         6 . The method of claims  1  or  2 , where administering comprises administering a CXCR4 antagonist with a STAT3 activator and an agent that increases nitric oxide content. 
     
     
         7 . (canceled) 
     
     
         8 . (canceled) 
     
     
         9 . (canceled) 
     
     
         10 . The method of claim  9 , wherein said one or more nerve growth factors are neurotrophic (NGF, BDNG, NT-3), glial-derived (GDNF) and/or pleotropic (PTN, VEGF). 
     
     
         11 . (canceled) 
     
     
         12 . (canceled) 
     
     
         13 . (canceled) 
     
     
         14 . (canceled) 
     
     
         15 . The method of  claims 4-6 , wherein the CXCR4 antagonist is administered after both the STAT3 activator or the agent that increases nitric oxide content. 
     
     
         16 . The method of  claim 6 , wherein the CXCR4 antagonist is administered between the STAT3 activator and the agent that increases nitric oxide content. 
     
     
         17 . (canceled) 
     
     
         18 . (canceled) 
     
     
         19 , the method of claim  17 , wherein said peripheral nerve deficit is due to trauma or an iatrogenic event. 
     
     
         20 . The method of claim  17 , wherein said peripheral nerve deficit is due to infection. 
     
     
         21 . The method of claim  17 , wherein said peripheral nerve deficit is due to autoimmune disease. 
     
     
         22 . (canceled) 
     
     
         23 . (canceled) 
     
     
         24 . (canceled) 
     
     
         25 . The method of claim  23 , wherein said spinal nerve deficit is due to trauma or an iatrogenic event. 
     
     
         26 . The method of claim  23 , wherein said spinal nerve deficit is due to infection. 
     
     
         27 . The method of claim  23 , wherein said spinal nerve deficit is due to autoimmune disease. 
     
     
         28 . The method of claim  23 , wherein said spinal nerve deficit is a cervical deficit. 
     
     
         29 . The method of claim  23 , wherein said spinal nerve deficit is a lumbosacral deficit. 
     
     
         30 . The method of claim  23 , wherein said spinal nerve deficit is a thoracic deficit. 
     
     
         31 . (canceled) 
     
     
         32 . (canceled) 
     
     
         33 . (canceled) 
     
     
         34 . (canceled) 
     
     
         35 . The method of claim  34 , wherein sensory function is nociceptive function. 
     
     
         36 . The method of claim  34 , wherein sensory function is mechanoceptive function. 
     
     
         37 . (canceled) 
     
     
         38 . The method of claim  37 , wherein motor control is fine motor control. 
     
     
         39 . The method of claim  37 , wherein motor control is gross motor control. 
     
     
         40 . (canceled)